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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In anesthetized, artificially ventilated dogs, the intracranial cerebrospinal fluid (CSF) pulse waves were studied simultaneously with the central aortic pressure, central venous pressure (CVP), and the sagital sinus pressure under physiological conditions and in normovolemic arterial hypotension and hypertension, in acute cardiac insufficiency of the right atrium, in raised intracranial pressure (ICP), and in arterial hypoxemia. The physiological CSF pulsations are shown to be mainly arterial in origin. In the diastolic phase, the descending part of the pulse curve can be modified by venous superpositions coinciding with the right atrial "A" wave. With increase of ICP the configuration of the CSF pulsations changes: the venous superpositions disappear and the waves become more and more arterial in shape. Furthermore, the pulse amplitude increases considerably. The same change can be observed when cerebral vessels are dilated by arterial hypoxemia. During cardiac insufficiency and consecutive increase of CVP, the CSF pulse curve is venous in shape and the right atrial "A" wabe predominates. In arterial hypotension, CSF pressure decreased. Conversely, in angiotensin-induced systemic arterial hypertension, CSF pressure and its pulse amplitude increased. It is concluded that both systemic arterial blood pressure and cerebrovascular reactivity are major determinants for the shape and the pressure amplitude of the intracranial CSF pulse waves. In the presence of cerebral vasodilatation, systemic arterial blood pressure may be an important factor in raising ICP and altering the brain tissue compliance, because cerebral vascular damping of the arterial pulse is diminished and the arterial pressure head may be directly transmitted to the cerebral capillary bed.
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PMID:Influence of systemic and cerebral vascular factors on the cerebrospinal fluid pulse waves. 83 Aug 13

A mean decrease of 60% in liver blood volume was recorded by a plethysmographic technique during electrical stimulation of the hepatic nerves in anesthetized, vagotomized dogs. A decrease in pressure in the vascularly isolated carotid sinus to 40 mm Hg, from a mean control of 144 mm Hg, decreased liver blood volume by a mean of 16%; arterial blood pressure increased by a mean of 77 mm Hg. Carotid sinus hypotension was accompanied by respective mean increases of 16% and 1.4% in hepatic arterial and portal venous blood flows, and of 45% and 22% in arterial and portal resistances. Increase in sinus pressure to 240 mm Hg increased liver blood volume by a mean of 20%; arterial blood pressure decreased by 90 mm Hg. Sinus hypertension was accompanied by respective mean decreased of 10% and 1.5% in hepatic arterial and portal venous blood flows, and of 44% and 18% in arterial and portal resistances. Interruption of afferent vagal traffic from cardiopulmonary receptors was maximally effective in decreasing liver blood volume at a carotid sinus pressure of 40 mm Hg and was ineffective at carotid sinus pressures greater than 160 mm Hg. Combined withdrawal of carotid and cardiopulmonary vasomotor inhibition decreased liver blood volume by 42%; of this 37% was due to the cardiopulmonary and 63% to the carotid baroreflex. The study showed the canine liver to function as a blood reservoir by active mobilization of a portion of its blood volume.
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PMID:Change in liver blood flow and blood content in dogs during direct and reflex alteration of hepatic sympathetic nerve activity. 84 41

The concept that reflex control of cerebral vessels is unimportant has been challenged by recent studies which suggest that carotid baroreceptors have an important role in regulation of cerebral blood flow (CBF). In this study we have tested the hypothesis that arterial baroreceptors contribute to regulation of total or regional CBF. CBF was measured in anesthetized dogs with 15 mu microspheres. Stimulation of carotid baroreceptors, by raising carotid sinus pressure, did not alter or redistribute cerebral flow. Responses to baroreceptor stimulation were intact, as manifested by vasodilation in skeletal muscle. CBF decreased during systemic hypocapnia and increased during hypercapnia, which indicates that failure of cerebral flow to change during baroreceptor stimulation was not due to unresponsiveness of cerebral vessels. During hypercapnia, baroreceptor stimulation also failed to alter CBF. In other studies CBF was measured during increases in systemic arterial pressure, before and after denervation of arterial baroreceptors. Increases in arterial pressure did not increase CBF either before or after denervation of baroreceptors. We conclude that baroreceptor stimulation does not alter total or regional CBF and that baroreceptors do not regulate cerebral flow during systemic hypertension.
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PMID:Total and regional cerebral blood flow during stimulation of carotid baroreceptors. 94 13

We have previously demonstrated that baroreceptor discharge sensitivity is depressed in dogs with experimental heart failure and that this depressed sensitivity can be reversed by the Na+,K(+)-ATPase inhibitor ouabain. This suggests that enhanced Na+,K(+)-ATPase activity in baroreceptors is responsible for the blunted baroreceptor discharge sensitivity seen in heart failure state. Because aldosterone, a known stimulator of Na+,K(+)-ATPase, is elevated in heart failure the present study was undertaken to determine the effects on baroreceptor discharge of perfusion of the carotid sinus with aldosterone in normotensive dogs. Single unit baroreceptor activity was recorded as well as carotid sinus pressure and the diameter of the carotid sinus. Perfusion of the carotid sinus with aldosterone (in Krebs-Henseleit solution) significantly elevated threshold pressure (108.5 +/- 3.1 mm Hg versus 92.7 +/- 4.6 mm Hg, p less than 0.05) and reduced peak discharge rate (40.3 +/- 3.9 spikes/sec, p less than 0.05). These effects appeared 15 minutes after aldosterone perfusion and remained constant for the next 60 minutes. There was no change in the carotid sinus pressure-diameter curve during perfusion with aldosterone. Perfusion of the carotid sinus with ouabain (0.1 microgram/ml) during aldosterone perfusion did not reverse the blunted baroreceptor discharge. The blunted baroreceptor activity induced by perfusion of the carotid sinus with aldosterone was prevented by removal of the endothelial cells in the carotid sinus area with a balloon-tipped catheter or by perfusion with saponin. Finally, perfusion of the carotid sinus with spironolactone (10 ng/ml), a mineralocorticoid receptor antagonist, prevented the inhibitory effect of aldosterone. These data suggest that aldosterone reduces maximum baroreceptor discharge.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1992 Mar
PMID:Aldosterone reduces baroreceptor discharge in the dog. 154 52

To examine CSF hydrodynamics, we studied 16 patients with idiopathic intracranial hypertension and 45 control subjects with a constant-pressure infusion method. Fifteen patients had 155 examinations up to 15 years after the onset of disease. In most patients, the disturbances of CSF hydrodynamics persisted for many years. We identified at least two mechanisms for the development of the increased CSF pressure: a rise of sagittal sinus pressure, probably explained by extracellular edema causing partial compression of the major venous sinus (type 1), or a low conductance with a compensatory increase in CSF pressure in order to sustain the bulk flow (type 2).
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PMID:CSF hydrodynamics in idiopathic intracranial hypertension: a long-term study. 156 41

The hypothesis that changes in baroreflex function seen in hypertension could be explained by a decreased vascular compliance in the carotid sinus region itself was tested. Six dogs were made chronically hypertensive (MAP = 146.0 +/- 3.3 mm Hg) using a bilateral renal wrap technique, while six other dogs were sham operated and served as normotensive controls (MAP = 125.8 +/- 4.7 mm Hg). Six weeks after the procedure, compliance of the carotid sinus region was measured, and carotid baroreflex control of arterial pressure and heart rate was assessed acutely. Dogs were anesthetized with sodium pentobarbital and the carotid sinus was isolated and perfused at controlled pressures. Vagotomy was performed to eliminate aortic and cardiopulmonary reflex buffering. The carotid sinus pressure (CSP) was changed from 25 to 250 mm Hg in a stepwise fashion, and the corresponding arterial pressure, heart rate and volume changes were recorded. Compliance was determined as the change in volume infused divided by the changes in pressure achieved. Significant differences between the normotensive and hypertensive groups were found in the reflex responses of arterial pressure and heart rate to changes in CSP. Carotid sinus compliance decreased with increasing CSP, but was not different in the two groups. Changes in baroreflex responses seen in mild hypertension occur without significant changes in carotid sinus compliance, and cannot be explained solely by a decreased compliance in the receptor wall.
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PMID:Carotid sinus compliance and baroreflex responses in hypertensive dogs. 193 Aug 51

67 patients with benign intracranial hypertension (BIH) and 44 with normal pressure hydrocephalus (NPH) were examined by employment of infusion tests. Brain swelling (decrease of ventricular size with normal or increased brain tissue density) was a characteristic feature of BIH. It may result from venous outflow disturbances leading to vascular engorgement. But later, the process appears to be independent from the increase of the dural sinus pressure. This was normal in patients with BIH and NPH. Despite absorption disturbances there was a strong positive correlation in NPH between cerebrospinal fluid- and dural sinus pressure, while in BIH such a correlation was absent. The data confirm a pathogenesis of brain swelling in BIH as an obstacle to venous outflow at the level of the bridging veins and venous lacunae, however, not at the level of the dural sinuses.
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PMID:Venous and cerebrospinal fluid outflow in patients with brain swelling and oedema. 208 38

Only 6 patients with intracranial hypertension associated with unruptured cerebral arteriovenous malformations have been reported. We report 6 additional patients seen at the Cleveland Clinic during the past 10 years. The average age was 28 years (range, 19-44 years); 4 were women. Symptoms and signs included papilledema (6 patients), headache (6), transient nonepileptic focal symptoms (4), visual obscurations (3), ipsilateral carotid or ocular bruits (3), abnormal visual fields (3), focal seizures (2), and progressive visual loss (1). Enhanced computed tomography (CT) or magnetic resonance imaging (MRI) demonstrated the malformations in all 6 patients. The malformations were large, supplied by the branches of the middle and anterior cerebral arteries, with the posterior cerebral artery contributing in 3 patients, and all drained into the superior sagittal sinus. Associated venous obstruction was seen in 2 patients. Four patients underwent excision of the arteriovenous malformation, with resolution of papilledema in all 4. Measurements of cortical arterial and venous pressures during surgery in 3 patients showed decreased feeding artery pressures and elevated draining vein pressures, which normalized after removal of the malformation. Treatment in the 2 remaining patients consisted of medical therapy (acetazolamide, furosemide, steroids) alone in 1 patient, and in conjunction with proton beam radiation in the other. Papilledema resolved in the former patient, but the patient receiving proton beam radiation still had papilledema 2 years later. Intracranial hypertension associated with unruptured cerebral arteriovenous malformations occurs in young patients with high flow malformations that drain into the superior sagittal sinus, and is likely the result of increased cortical venous and superior sagittal sinus pressure. Excision of the malformation effectively reduces the intracranial pressure.
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PMID:Intracranial hypertension associated with unruptured cerebral arteriovenous malformations. 219 10

The present study was designed to determine whether 12 wk of daily exercise alter autonomic neural control of the heart during baroreflex stimulation in healthy dogs. We studied 16 untrained and 12 endurance-trained anesthetized dogs which were instrumented to measure arterial blood pressure (AP), carotid sinus baroreceptor pressure (CBP), electrocardiogram (ECG), heart rate (HR), and R-R interval (RR). The arterial baroreflex was studied during hypertension caused by i.v. bolus infusion of phenylephrine, hypotension caused by i.v. bolus infusion of nitroprusside, and bilateral carotid occlusion (BCO) in which carotid sinus pressure was reduced to 41 +/- 2 mm Hg (mean +/- SEM). Arterial baroreflex sensitivity, which was assessed by determining the change in heart interval (i.e., change in RR) per unit change in systolic AP (delta RR/delta AP), was significantly lower during the hypertensive challenge in the trained dogs compared to the untrained dogs (2.2 +/- 0.3 vs 6.8 +/- 1.5 ms.mm Hg-1, respectively). Similarly, the delta RR/delta AP was substantially lower during the hypotensive challenge in trained dogs vs the untrained dogs (1.2 +/- 0.3 vs 1.8 +/- 0.4 ms.mm Hg-1, respectively). In addition, the HR response to the BCO was significantly less in trained dogs (22 +/- 2 bpm) vs untrained dogs (32 +/- 5 bpm). The open-loop gain (Go), which was used to quantitate the effectiveness of the carotid baroreflex to increase mean systemic AP during BCO, was similar in both untrained and trained dogs (2.9 +/- 0.6 and 2.4 +/- 0.5, respectively). These data indicate that, while endurance training significantly reduces the HR component of the arterial baroreflex, the arterial pressure response apparently is not altered.
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PMID:Endurance training alters arterial baroreflex function in dogs. 235 17

Changes of myocardial microvascular permeability in chronic renovascular arterial hypertension were studied. Hypertension was induced in dogs utilizing a one-kidney, one-clip Goldblatt model. Systemic arterial pressure, coronary sinus pressure, systemic venous pressure, myocardial lymph flow rate, myocardial interstitial fluid pressure, and the lymph-to-plasma protein concentration ratio for total plasma proteins and for beta-lipoprotein (CL/CP) were determined in control animals and 4-6 weeks following the Goldblatt procedure in hypertensive animals. Control values for the normotensive animals were 123 +/- 17 mm Hg, 7.3 +/- 1.3 mm Hg, 2.5 +/- 2.1 mm Hg, 3.1 +/- 2.1 ml/hr, 14.9 +/- 3.1 mm Hg, 0.82, and 0.33, respectively, while control values for the chronically hypertensive dogs were 160 +/- 20 mm Hg, 7.8 +/- 1.9 mm Hg, 2.9 +/- 2.5 mm Hg, 10.5 +/- 2.5 ml/hr, 24.8 +/- 3.7 mm Hg, 0.87, and 0.31, respectively. Under control conditions, myocardial lymph flow rate was significantly higher in the hypertensive group while no difference could be demonstrated in CL/CP between the two groups. This is indicative of either a change in myocardial microvascular permeability or an increase in microvascular exchange surface area. Coronary sinus pressure was elevated in both groups in order to increase transmicrovascular fluid flux and determine the filtration-independent reflection coefficient (sigma) for each group. Sigma is a surface area-independent indicator of microvascular permeability when determined for specific protein molecules at high transmicrovascular fluid fluxes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Microvascular changes in the heart during chronic arterial hypertension. 335 78


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